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991.
992.
Jing Feng Xin Chen Rui Liu Changkui Cao Wei Zhang Yang Zhao 《Free radical research》2018,52(8):840-849
Myocardial ischemia–reperfusion (MI/R) injury is a crucial cause for mortality throughout the world. Recent studies indicated that melatonin might exert profound cardio-protective effect in MI/R injury. However, the underlying mechanisms are not completely understood. In the current study, we aimed to explore the potential effect of melatonin in the pathological process of MI/R. Both in vivo MI/R model and in vitro H9c2 cell line simulated I/R (SIR) model were applied with or without melatonin supplementation. We found that Sirtuin3 (Sirt3) expression and activity were markedly decreased under MI/R and SIR conditions. Melatonin treatment significantly increased myocardial Sirt3 expression, and alleviated MI/R-induced cardiac morphology changes and cardiac dysfunction, as well as myocardial apoptosis level. In addition, DHE and JC-1 staining results demonstrated that melatonin reduced mitochondrial reactive oxygen species (ROS) generation and restored ATP production after SIR injury via elevating Sirt3 expression. By using siRNA targeting Sirt3, we confirmed that the beneficial effects of melatonin were dependent on Sirt3, which in turn deacetylated and activated manganese superoxide dismutase (MnSOD). Collectively, the current study demonstrated the protective effect of melatonin against MI/R injury via alleviating myocardial oxidative stress. Moreover, these beneficial effects were associated with the deacetylation modification of Sirt3 on MnSOD. 相似文献
993.
Yanchun Liang Hongyu Xie Jinjie Wu Duo Liu Shuzhong Yao 《Reproductive biology and endocrinology : RB&E》2018,16(1):122
Endometriosis is a complex and heterogeneous disorder with unknown etiology. Dysregulation of macrophages and innervation are important factors influencing the pathogenesis of endometriosis-associated pain. It is known to be an estrogen-dependent disease, estrogen can promote secretion of chemokines from peripheral nerves, enhancing the recruitment and polarization of macrophages in endometriotic tissue. Macrophages have a role in the expression of multiple nerve growth factors (NGF), which mediates the imbalance of neurogenesis in an estrogen-dependent manner. Under the influence of estrogen, co-existence of macrophages and nerves induces an innovative neuro-immune communication. Persistent stimulation by inflammatory cytokines from macrophages on nociceptors of peripheral nerves aggravates neuroinflammation through the release of inflammatory neurotransmitters. This neuro-immune interaction regulated by estrogen sensitizes peripheral nerves, leading to neuropathic pain in endometriosis. The aim of this review is to highlight the significance of estrogen in the interaction between macrophages and nerve fibers, and to suggest a potentially valuable therapeutic target for endometriosis-associated pain. 相似文献
994.
Padhiar Arshad Ahmed Chanda Warren Joseph Thomson Patrick Guo Xuefang Liu Min Sha Li Batool Samana Gao Yifan Zhang Wei Huang Min Zhong Mintao 《Applied microbiology and biotechnology》2018,102(5):2363-2377
Applied Microbiology and Biotechnology - The formation of inclusion bodies (IBs) is considered as an Achilles heel of heterologous protein expression in bacterial hosts. Wide array of techniques... 相似文献
995.
Zhang Weibin Xu Jingnan Liu Dan Liu Huan Lu Xinzhi Yu Wengong 《Applied microbiology and biotechnology》2018,102(5):2203-2212
Applied Microbiology and Biotechnology - It has been a long time since the first α-agarase was discovered. However, only two α-agarases have been cloned and partially characterized so far... 相似文献
996.
Zou Shu-Ping Zheng Yu-Guo Wu Qun Wang Zhi-Cai Xue Ya-Ping Liu Zhi-Qiang 《Applied microbiology and biotechnology》2018,102(2):733-742
Applied Microbiology and Biotechnology - Enantioselective hydrolysis of epoxides by epoxide hydrolase (EH) is one of the most attractive approaches for the synthesis of chiral epoxides. So far,... 相似文献
997.
Dengqun Liu Megan D Radyk Rebecca L Cunningham Joseph Burclaff Greg Sibbel Hei‐Yong G Lo Valerie Blanc Nicholas O Davidson Zhen‐Ning Wang Jason C Mills 《The EMBO journal》2018,37(7)
In 1900, Adami speculated that a sequence of context‐independent energetic and structural changes governed the reversion of differentiated cells to a proliferative, regenerative state. Accordingly, we show here that differentiated cells in diverse organs become proliferative via a shared program. Metaplasia‐inducing injury caused both gastric chief and pancreatic acinar cells to decrease mTORC1 activity and massively upregulate lysosomes/autophagosomes; then increase damage associated metaplastic genes such as Sox9; and finally reactivate mTORC1 and re‐enter the cell cycle. Blocking mTORC1 permitted autophagy and metaplastic gene induction but blocked cell cycle re‐entry at S‐phase. In kidney and liver regeneration and in human gastric metaplasia, mTORC1 also correlated with proliferation. In lysosome‐defective Gnptab?/? mice, both metaplasia‐associated gene expression changes and mTORC1‐mediated proliferation were deficient in pancreas and stomach. Our findings indicate differentiated cells become proliferative using a sequential program with intervening checkpoints: (i) differentiated cell structure degradation; (ii) metaplasia‐ or progenitor‐associated gene induction; (iii) cell cycle re‐entry. We propose this program, which we term “paligenosis”, is a fundamental process, like apoptosis, available to differentiated cells to fuel regeneration following injury. 相似文献
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